To: scaram(o)uche who wrote (8407 ) 5/20/2003 2:43:31 AM From: Miljenko Zuanic Respond to of 52153 While we do not have real data from Avastin CC trial, one can assume that this was break-true for anti-angiogenesis approach. More importantly, support one of the two proposed hypothesis how cancer cells growth neovasculature. More probably, because Avastin neutralize circulating VEGF, it is hypothesis that microvessel sprouting is from outside toward inside (destabilization of the existing capillaries, break down and growth/connection toward tumor mass), than opposite. That cancer cells secrete VEGF and initiate new vessel growth from inside, toward existing capillaries. This is very interesting for REGN. VEGF and Angio-2 work in co-operation during early stage of the new capillary growth. Avastin trials was for naive metastatic CC, so it point out that anti-angio approach may work better as initial early therapy, than for refractory and progressed cancer (when one do not need many new capillaries). This was in line with breast cancer failure. Bottom line, it may not be that difference from cancer to cancer type, more likely depending on timing and combination, imo. What this means for biosector? DNA is on forefront of the molecular biology research, for years. Premier research machine. It points out that we are still at early stage of the understanding how and when diseases develop, and how to threat it successfully. Plenty of room for new advances, in many disease categories. Another interesting thing is that DNA is constantly pushing connection between rash and durability of the response (survival) for anti-EGF approach. Now I am tickled and curious (because I am bit conservative on Tarceva) how will Tarceva fire in early NSCLC? Miljenko